Dr. Yi-Ping Li
The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Integrative Biology and Pharmacology
Skeletal muscle is the largest organ of the human body with important functions that are not only mechanical but also metabolic. My lab is interested in the mechanisms of skeletal muscle remodeling, either positive or negative, in response to physiological and pathological stress. For example, many inflammatory diseases including cancer, AIDS, sepsis, diabetes, COPD and congestive heart failure induce debilitating muscle wasting due to loss of muscle mass (cachexia). On the other hand, diseased or injured muscle has the capacity to regenerate leading to recovery of muscle mass and function. We are currently working on two research areas.
1. Mechanism of skeletal muscle wasting We currently focus on the role of specific signaling events activated by inflammation mediators involving Toll-like receptors and p38b MAPK in mediating muscle wasting in various disease models including cancer, sepsis and diabetes. Our strategy is to identify the transcription factors regulated by these signaling events and their respective target genes in the ubiquitin-proteasome and the autophagy-lysosome pathways that degrade muscle proteins. We also try to identify the humoral factors that activate the above described proteolysis systems in cachectic diseases. Collaborations with clinical scientists are underway to translate our basic research findings into clinical interventions of cachexia.
2. Regulation of skeletal muscle regeneration Skeletal muscle adapts to various stresses (injury, disease and training) by regenerating to make new muscle (myogenesis). Muscle regeneration is the function of muscle stem cells (also known as satellite cells) that have the capacity to proliferate, differentiate and fuse to form new muscle fibers when stimulated by myogenic cues. We study how these cells sense chemical or mechanical cues for regeneration through their plasma membrane receptors and activate specific intracellular signaling pathways that initiate muscle specific gene expression.